The Most Common Disease That Causes Loss of Teeth – Dental Caries Part 10

You can read part 9 of most common disease before reading part 10.

As noted earlier in this article, the initial attack on enamel appears to be by highly mobile hydrogen ions permeating the organic matrix enabling them to attack the surface of the apatite crystals. The apatite crystals become progressively smaller. Microdissection of the translucent zone has shown that the apatite crystals have declined in diameter from the normal of 35-40 nm to 25-30 nm and in the body of the lesion to 10-30 nm. In the dark zone, by contrast, enamel crystals appeared to have grown to 50-100 nm and in the surface zone to 35-40 nm. These findings also suggest that demineralization and remineralization are alternating processes.

However, as the lesion progresses and cavitation develops, demineralization comes to dominate the process. In broad general terms therefore, enamel crystallites are progressively dissolved until disintegration becomes visible microscopically. Defects eventually become large enough to allow bacteria to enter.

There is evidence of preferential destruction of the prism cores, and experimentally a similar effect is seen when enamel is exposed to dilute acid.

Chalky enamel. An electronphotomicrograph of chalky enamel produced by the action of very dilute acid. The crystallites of calcium salts remain intact in the prism sheaths, while the prism cores and some of the interprismatic substance have been destroyed. The same appearance is seen in chalky enamel caused by early caries

Whatever the precise nature of these changes, bacteria do not physically penetrate enamel until acid destruction of the tissue has provided pathways large enough for them to enter.

Early cavitation in enamel caries. The surface layer of the white spot lesion has broken down, allowing plaque bacteria into the enamel.

Once bacteria have penetrated the enamel they reach the amelodentinal junction and spread laterally to undermine the enamel. This has three major effects. First, the enamel loses the support of the dentine and is therefore greatly weakened. Second, it is attacked from beneath.

Enamel caries. Infection has spread along the amelodentinal junction undermining and invading the deep surface of the enamel. The terminations of the dentinal tubules are also infected but destruction, at this stage, is mainly at the expense of the enamel

Third, spread of bacteria along the amelodentinal junction allows them to attack the dentine over a wide area. Thus the primary lesion provides the bridgehead for the attack on enamel, but undermining of the enamel determines the area of a cavity. Clinically this is frequently evident when there is no more than a pinhole lesion in an occlusal pit, but cutting away the surrounding enamel shows it to be widely undermined.

As undermining of the enamel continues, it starts to collapse under the stress of mastication and to fragment around the edge of the (clinically obvious) cavity. By this stage, bacterial damage to the dentine is extensive.

The initial (non-bacterial) lesion forms deep to carious enamel before a cavity has formed. Diffusion of acid into the dentine leaves its collagenous matrix intact at this stage. However, once bacteria have penetrated the enamel, they spread along the amelodentinal junction to attack the dentine over a wide area. The lesion is therefore conical with its apex towards the pulp.

The infected lesion is facilitated by the dentinal tubules which form a pathway open to bacteria. After demineralization, the dentine matrix is progressively destroyed by proteolysis. Streptococci play the major role in the attack on enamel, but lactobacilli may be as important in dentine caries. As the lesion progresses, the bacterial population becomes increasingly mixed and their relative contributions to dentine destruction become more difficult to disentangle.

At first, the decalcified dentine retains its normal morphology, and no bacteria can be seen. Once bacteria have reached the amelodentinal junction they extend down the tubules, soon fill them and spread along any lateral branches. The tubules become distended into spindle shapes by the expanding masses of bacteria and their products, which the softened matrix cannot confine. As a result, adjacent less heavily infected tubules become bent. Later still, the intervening tubule walls are destroyed and collections of bacteria in adjacent tubules coalesce to form irregular liquefaction foci. These in turn coalesce to form progressively more widespread tissue destruction.

Caries of dentine. Infected tubules and fusiform masses of bacteria have expanded into the softened tissue. Adjacent tubules in the demineralized dentine have been bent and pushed aside by these masses.

Advanced dentine caries. The dentine is disintegrating (left). To the right is a large liquefaction focus and tubules packed with bacteria.

In some areas bacteria also spread laterally, and, occasionally, large bacteria-filled clefts form at right angles to the general direction of the tubules. Clinically, these clefts may allow carious dentine sometimes to be excavated in flakes in a plane parallel to the surface.

Clefts in carious dentine. Infection is tracking along the tubules but has also spread across the tubules, forming heavily infected clefts. The appearances suggest that there are lines of weakness in the dentine, along which infection spreads easily

Continue reading Part 11.